The GEM-GBMs initiate in adult glial fibrillary acidic protein (GFAP)-expressing glial progenitor populations (mainly astrocytes), with dominant inactivation of RB tumor suppression, and progress to GBM upon induction of the constitutively active mutant KRASG12D and deletion of PTEN alleles, followed by spontaneous somatic p53 missense mutations. The gene discussed is TP53; the disease is neoplasm.